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BS127: AIDs > Lectures 1-14 > Flashcards

Lectures 1-14 Flashcards

1
Q

What are the 3 domains of life?

A

Archaea, Bacteria and Eukarya.

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2
Q

How do bacteria multiply?

A

Asexual reproduction by binary fission or budding. Cells double in size and then split in two.

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3
Q

Describe the 4 points of a bacterial growth curve.

A

Lag Phase, Log Phase, Stationary Phase, Death Phase.

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4
Q

What are examples of how to measure growth in bacteria?

A

Cell number, optical density, fresh/dry weight, protein and DNA.

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5
Q

What is selective media?

A

A media which allows the growth of some types of organisms.

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6
Q

What is differential media?

A

A media which allows the identification of organisms based on growth and appearance of that medium.

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7
Q

What is ApiZym?

A

A test for pathogens. A culture is grown, suspended in a buffer and wells are inoculated. The resulting colour is compared to the database.

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8
Q

Definition of Species.

A

A group of strains that show a high degree of similarity and differ considerably from related strains.

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9
Q

What is phenotypical analysis?

A

Morphological, metabolic, physiological and chemical characteristics.

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10
Q

Define genotypic.

A

comparative at genome and gene levels.

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11
Q

Define phylogenetic.

A

Framework for evolutionary relationships.

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12
Q

Describe the staining procedure.

A

Spread culture over slide, dry and fix over flame.

Add stain and dry, add drop of oil.

Observe under a microscope.

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13
Q

How can genetic sequencing be achieved?

A

PCR, can amplify a section of DNA. Now use fluorescent dyes and a capillary column.

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14
Q

Tell me about Capsules.

A

Polysaccharides, slimy outer layer, loose polymer fibres that extend outwards.

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15
Q

3 types of capsules.

A

Glycocalyx involved in biofilm formation.

Capsule is an organised, tight matrix.

Slime layer is unorganised, doesn’t exclude small particles unlike capsule.

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16
Q

Role of Capsules.

A

Carbon storage, captures nutrients, protection, biofilms.

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17
Q

What is the S layer?

A

paracrystalline outer wall layer made from protein.

Protects against ion and pH fluctuations.

Sometimes a virulence factor.

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18
Q

What is in the peptidoglycan structure?

A

Residues include NAG and NAM.

Arranged in dimers, held by amide bonds.

Non-protein amino acids have D- handle.

They protect against degradation by proteases.

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19
Q

How is PG synthesised?

A

Chains of PG subunits joined by cross-links between peptides.

Carboxyl group of D-alanine connected to DAPA.

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20
Q

What is a Lysozyme?

A

Enzyme that degrades 1,4 glycosidic bonds.

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21
Q

How does penicillin inhibit PG synthesis?

A

Linker peptide has x2 D-Ala.

One cleaved during link w DAPA (transpeptidation).

Stops cell wall synthesis.

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22
Q

Describe the structure of teichoic acids.

A

Glycerol polymers joined by phosphate groups.

Covalently joined to peptidoglycans and plasma membranes.

Not found in Gram - bacteria.

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23
Q

How do archaeal cell walls differ to bacterial cell wall?

A

They have no peptidoglycan.

Has N-acetylalosaminuronic acid instead of N-acetylmuramic acid.

Linked by beta 1,3 not 1,4.

Not sensitive to Penicillin.

No D-amino acids in linker.

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24
Q

What are sterols/hopanoids?

A

Rigid Planar molecules that stabilise membrane structure.

Hop in bacteria, Sterol in Eukaryotes.

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25
Q

Describe Gram - outer cell membranes.

A

Asymmetric due to lipopolysaccharides.

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26
Q

What are the two ways in which OM is linked to the cell?

A

Braun’s lipoprotein. Covalently linked to peptidoglycan and embedded in OM by hydrophobic end.

Adhesion sites. Allows transport of substances to OM.

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27
Q

How are archaeal membranes different to the other two domain?

A

They have branched-chain hydrocarbons that attach to glycerol by ether links not fatty-acid links.

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28
Q

What are LPS?
What are the three main components of it?

A

Lipid and Carbohydrate molecules. (called endotoxin when free in host).
Lipid A
Core polysaccharide
O side chain

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29
Q

What is Lipid A?

A

x2 glucosamine residues linked to fatty acids and phosphates.
Present in OM.

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30
Q

What is core polysaccharide?

A

Side chains of NAG, phosphate and ethanolamine.
Can induce an immune response.

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31
Q

What is the O side chain?

A

Responsible for antigenic makeup of bacteria.

Flexible and bent.

Rough and smooth.

Defines specific receptor that bacteria will attach to (where it causes problems etc).

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32
Q

Function of LPS?

A

Lipid A stabilises OM.

Core polysaccharide is charged, reduces permeability of hydrophobic substances.

O-antigen needed to infect host.

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33
Q

What are endotoxins?

A

Act as prime immune system against pathogen.
Released during cell division or cell lysis.

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34
Q

LAL test.

A

Used to assay LPS. Contains a clotting factor that is released if contact made w bacterial cells.

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35
Q

What are the properties of endotoxins?

A

Heat stable
Toxic
Triggers release of cytokines
Activates TFs

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36
Q

What are porins?

A

Homotrimeric, transmembrane proteins.

Conserved structure.

Form water-filled channels in OM.
Most non-selective.

Resistant to protease.

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37
Q

What is the structure of porins?

A

16-stranded antiparallel beta-barrels.
Stable.
Salt-bridge between N and C terminal.

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38
Q

Enzyme Activity in Periplasm.

A

Nutrient acquisition.

Energy conservation.

Periplasmic binding proteins.
Chemoreceptors.

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39
Q

How is protein exported into the periplasm?

A

Sec Pathway: sends polypeptides through cytoplasmic membrane using translocase.

Folding of protein happens next.

TAT Pathway: sends folded enzymes across cytoplasmic membrane.

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40
Q

Structure of Flagella?

A

Ring structures, anchored to membrane.
Has antigenic properties.
Motor driven through proton transfer through ring structure.

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41
Q

Structure and Synthesis of flagellum filament?

A

Hook anchored to whole cell wall.
Has 4 rings.
Grows from tip, subunits made in cytoplasm.

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42
Q

What is different about Gram + flagella?

A

There are no L and P rings.
Anchor in the membrane layer is more complex.

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43
Q

Describe bacterial movement.

A

Run and tumble.
Anticlockwise motor rotation, followed by clockwise.

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44
Q

Chemotaxis: Biased random walk.

A

MCP (proteins) interact w cytoplasmic membranes.

Che proteins interact with rings.
Dictates run or tumble by switch from anti to clockwise.

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45
Q

Chemotaxis: signal recognition.

A

Signals recognised by MCP.
MCP interacts with sensor kinase CHeA.
Attractant = decrease in CheA
Repellent = increase in CheA.

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46
Q

Chemotaxis: motor switch.

A

CheA phosphorylates CheY-p.
Binding effects switch from anti to clockwise.

Phosphatase, CheZ, dephosphorylates CheY, anti resumes.

Attract = CheY-p decrease.
Repellent = CheY-p increase.

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47
Q

Chemotaxis: Adaptation.

A

CheR methylates MCP.

CheB is phosphorylated by CheA-p.
Low conc. attraction = high ChA/B-p. (demethylation of MCP, increase sensitivity to attractant).

High conc. attractant is opposite, increase autophosphorylation of CheA (tumble).

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48
Q

Gliding Motility.

A

3 Gld proteins are components of ABC transporter.

5 Gld lipoproteins in CM or OM.
Disruption of proteins leads to less motility.

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49
Q

Fimbriae/pili.

A

Adhesion to surfaces.
Deters virulence.
Antigenic.

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50
Q

Fimbriae/pili role in adhesion.

A

Allow bacterial cell to penetrate the mucus layer and attach itself to epithelial cell.

Sit on top of cell, change their metabolism.

Penetrate by going through junctions to less protected cells.

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51
Q

Describe Type 1 Fimbriae.

A

FimH binds to D-mannose.
FimF/G link FimH adhesion.
FimC is Chaperone.
FimD is usher protein.

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52
Q

P-pili.

A

Aka PAP. Similar to type 1.
PapG is tip adhesin.
3 types, PapG1,2,3.

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53
Q

Type 4 Pili. What do they do?

A

Aggregate to form bundles.
Host Cell adhesion.
Form Biofilm.
Twitching motility.

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54
Q

Species specificity of pathogens.

A

Determined by LPS.
CFA fimbriae present.
K99/K88 are fimbrial antigens.

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55
Q

E.coli adherence.

A

Via CFA (colonising factor antigen).
Pathogenic strains adhere to other tissues.
Non-pathogenic adhere to colon.

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56
Q

Describe the sex pilus.

A

aka F pilus.
Helical arrangement of pilin (TraA).
Attaches via tip, retracts to bring cell together.

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57
Q

What is conjugation.

A

Attachment of F+ donor to F- recipient.
Retraction.
Exchange.
Transformation both F+ cells.

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58
Q

What are the stages of sporulation.

A

Cell under stress.
DNA organised along cell axis.
A copy is moved to one side of cell, to capture in small part.
CM engulfs forespore in 2nd membrane.
Cortex removes water.
Exosporium produced.
Spore develops w cortical layers.
Original cell lyses.

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59
Q

Structure and Resistance of Endospores.

A

Thin outer layer of proteins, exosporium.
Spore coats w specific proteins.
Dehydration prevents denaturing.

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60
Q

What is Germination?

A

Uptake of water and amino acids.
Gram negative on release, but become positive as peptidoglycan layer is built up.

61
Q

What are virulence factors?

A

Determined by factors that aid in adhesion, antiphagocytic activity and toxin production.

62
Q

Example of Beta Lactams.

A

Penicillin.

63
Q

Example of Macrolides.

A

Erythromycin. (inhibit protein synthesis).

64
Q

Example of Fluoroquinolones.

A

Ciprofloxacin. (inhibit DNA gyrase).

65
Q

Example of tetracyclines.

A

Tetracycline. (inhibit protein synthesis).

66
Q

Example of Aminoglycosides.

A

Kanamycin. (inhibits protein synthesis).

67
Q

what does Tetanus Toxin do in the body?

A

Tetanospasmin.
A chain is neurotoxin.
B chain binds to gangliosides.
Released by cell lysis, targets CNS.
Halts release of glycine and GABA NTs.

68
Q

Streptococcus pneumonia.

A

Gram +
90 sterotypes (bacteria recognised by antibodies).
Competes w H. Influenza by attacking it w hydrogen peroxide.
Influ responds by signalling to our immune system to attack S. Pneu

69
Q

Clostridium Tetani.

A

Gram +
Spores are resistant to heat
Produces tatanospasmin.

70
Q

Rapid evolution of HIV by mutation.

A

HIV has RNA genome associated with reverse transcriptase.
Mutation rate 1 in 10,000 bases.

71
Q

What is antigenic variation/shift?

A

A virulence strategy.
They alter their surface proteins to avoid immune responses.
They can’t be killed by immune system anymore.

72
Q

Life cycle of Plasmodium falciparum.

A

Infection of RBC.
Gametocytes.
Bite.
Gamete
Zygote.
Gut invasion.
Sporozoites in salivary glands.
Bite.
Replication in liver.

73
Q

Adaptive immune response memory.

A

Primary response takes 7-10 days.
Secondary response much more powerful.
Memory improves the secondary response.

74
Q

Recognition of self and non self and altered self.

A

Typical non-self:
cell wall, proteins, carbohydrates, pathogen DNA, viral antigens.

Altered-self processes include malignant cells, apoptosis and oxidised proteins.

75
Q

What are examples of tissue specific responses?

A

Lungs have a mucus layer containing surfactant that reduces surface tension.

Skin is dry and keratinised.

Blood Briain Barrier (BBB) seperates blood from brain fluid. Tight junctions around the brain so antibodies cannot get up there.

76
Q

Examples of levels of response.

A

C3 deficiency, leads to repeated infections.
Pathogens that target immune cells, result in immunodeficiency.
Clinically-induced immunosuppression post-transplant increases vulnerability.
Autoimmunity from impaired regulation of powerful immune responses.

77
Q

Innate and Adaptive arms of the immune system.

A

Innate:
First line of rapid defence. No memory and non-specific. Encoded in the germ line.

Adaptive:
Slow to adapt, highly specific and has memory

78
Q

Cell-mediated and humoural mechanisms.

A

Cell-mediated immunity: defence provided by specialised cells in blood and tissues.

Humoural immunity: soluble-phase defence provided by secreted protein in body fluids.

79
Q

Innate Immune system structure.

A

Humoural: (chemical warfare)
Barriers
Defensins
Complement

Cell-mediated:
Phagocytic cells
Natural killer cells
TLRs (call for help)

80
Q

What are the 3 lines of Innate Immune System Defense?

A

Barriers

Cell-intrinsic responses

Specialised proteins and specialised cells

81
Q

Tell me about the barriers.

A

Thick layer of keratinised dead cells.
Tight junctions between epithelial cells.
Acidic stomach pH.
Mucus layers.

82
Q

Tell me about cell-intrinsic responses.

A

pathogen-induced phagocytosis.

degradation of dsRNA.

83
Q

Tell me about specialised proteins and specialised cells.

A

Professional phagocytes
NK cells
The complement system.

84
Q

Tell me about the mucus layer.

A

Made up of mucins and glycoproteins.
Slippery - hard for pathogens to attach.
Sugars on the branches are very soluble, hold lots of water.

85
Q

What are defensins found in the mucus layer?

A

Small, + charged antimicrobial peptides.
Hydrophobic or amphipathic helical domains.
(+ charge on one side, hydrophobic on the other side).

86
Q

How do defensins work?

A

Their helices may enter the core of the lipid and destabilise it.
They are more active on membranes without cholesterol, so do not lyse our own cells.

87
Q

Pathogen-Associate Molecular Patterns (PAMPs).

A

Needed when pathogen breaches our epithelial barriers.
Recognised by components of the complement system.

^perfoms direct killing and aids phagocytosis.

88
Q

How does Complement Activation target pathogens for Lysis? (Part 1)

A

Proenzymes activate next member in line by cleavage - amplified proteolytic cascade.

C3 into C3a and C3b cleavage is most important.

C3a calls for help. Inflammation stimulated by attracting phagocytes and lymphocytes.

C3b binds covalently to pathogen plasma membrane.

89
Q

What is involved in the lectin pathway?

A

Mannose and fructose binding proteins.

90
Q

What is involved in the alternative pathway?

A

Pathogen surfaces.

91
Q

C2 is currently inactive at this stage, how is it activated? What happens once this occurs?

A

C2 bumps into mannose or fructose to become activated.

It then lyses into two parts and cleaves C4.

92
Q

How does Complement Activation targets pathogens for Lysis? (Part 2)

This is an enzymatic process, there is amplification at every point. The process cleaves the protein and activates them.

A

Pathogen-bound C3b stimulates reactions C5-C8 at the marked membrane.

C9 is inserted into the membrane.

C9 pore breaches the membrane (C9 multimers form a membrane-attack complex).

Pathogen lysis.

93
Q

What are TLRs (Toll-like Receptors)?

A

A trans-membrane protein with leucine-rich repeats that are versatile binding motifs.

Binding to pathogenic fungi sends a signal to the nucleus, antifungal defensins expressed.

94
Q

How TLRs are like an alarm system?

A

TLRs on cell membranes of epithelial cells and macrophages, dendritic cells and neutrophils.

Signals to the nucleus after binding, transcription of pro-inflammatory genes and interferon response.

95
Q

What are the 3 main classes of phagocyte?

A

Neutrophil
Eosinophil
Macrophage

96
Q

What are Granulocytes?

A

Neutrophils and Eosinophils

Their cytoplasm is granular, they contain lysosomes and secretory vesicles

Macrophages are monocytes

97
Q

Describe Neutrophils

A

Many lobes

They phagocytose and destroy microorganisms

Recruited by macrophages, C3a and PAMPs

Abundant and short-lived.

98
Q

Describe Macrophages

A

Larger and longer life span than neutrophils

They engulf and digest dead or damaged cells

Can engulf protozoa

99
Q

Describe Eosinophils

A

Destroy parasites

Modulate allergic inflammatory responses

100
Q

How do phagocytes engulf their targets?

A

Display cell-surface receptors

Find signals, move to them and destroy pathogen

TLRs, Antibody receptors and C3b

Binding of ligands to these^ activates phagocytes

Causes killing and release of cytokines to attract more wbc.

Induces actin polymerisation

101
Q

How are the granules designed to attack pathogens? (An impressive armory)

A

Membrane-bound lysosomal derivatives.

Fuse with the phagosome membrane an release their contents to digest pathogen cell wall.

Defensins destabilise the membranes.

102
Q

What is the short story of how the ‘armory’ works?

A

Cells come in

membranes attacked by defensins

cell membranes attacked by the complement

enymes/defensins sprayed onto the cell once granules have fused with the phagosome

respiratory burst makes oxygen species to throw at the pathogen.

103
Q

Which phagocyte is known as the suicide squad?

A

Neutrophils, they usually die in the killing frenzy

They use their own DNA to eject a sticky web that traps pathogens, preventing their escape.

104
Q

How can some bacteria survive the killing frenzy?

A

Addition of sialic acid to capsule components avoids complement attack and subsequent engulfment.

Some bacteria replicate inside neutrophils by expressing virulence factors that protect against respiratory burst.

Some bacteria can neutralise actin polymerisation and phagocytosis by injecting a toxin that disrupts actin cytoskeleton formation.

Some bacteria hide inside macrophages - little bitches

105
Q

How does inflammation aid the killing frenzy?

A

Blood vessels dilate, swelling and accumulation of complement cascade components.

TLR and activated macrophages contribute, secrete cytokines.

106
Q

What can go wrong with inflammation?

A

Release of cytokines, excessive blood vessel dilation, lowers blood pressure.

107
Q

What does the innate immune system rely on?

A

Recognition of CpG motifs in viral DNA by TLR9.

Recognition of viral dsDNA.

108
Q

What are Interferons?

A

Cytokines, induced by dsRNA.

IFN-alpha and IFN-beta

Induce changes in infected cells (autocrine action) and neighbouring cells (paracrine action).

109
Q

How do IFNs limit viral replication?

A

Limit spread of virus,

warn neighbouring cells of infection, cytokine inducing,

activate ssRNA nuclease which degrades host ssRNA non-specifically.

inhibit translation.

promoting apoptosis.

regulate display of viral peptides on OM, provides signals for T cells.

Stimulates expression of immunoproteasome to destroy viral proteins.

attract NKCs and activate macrophages.

110
Q

What are Natural Killer Cells?

A

NK cells recognise their targets by monitoring the level of expression of immune system recognition molecules.

Attracted to virally-infected cells by IFNs.

NK cells persuade these cells to commit suicide. APOPTOSIS.

111
Q

How do NK cells trigger apoptosis?

A

Apoptotic signals given.

Mild convolution chromatin compaction.
Cytoplasmic condensation.

Nuclear fragmentation and cell fragmentation.

Phagocytosis.

112
Q

what is special about the adaptive immune system?

A

Can provide protection against pathogens that have never been encountered before.

Highly specific

Long-lasting protection

113
Q

Describe dendritic cells

A

Have lots of TLRs

Activated by binding of pathogen to receptor

phagocytose and degrade invading microorganisms

Peptides displayed on the surface

114
Q

How do dendritic cells work?

A

Innate immune response activates DC, engulf their prey.

Digest pathogen into peptides while moving to lymphoid

Mature from DC into APC, displaying peptides on the cell surface.

Peptides presented to T cells.

115
Q

How do T cells develop?

A

In thymus tissue from thymocytes, derived from common lymphoid progenitor cells, which themselves are derived from haemopoietic stem cells.

116
Q

How do DC activate T cells?

A

DC shows peptides to T cells.

T cell TCR recognises ‘self’ antigen, no action taken.

T cell TCR recognises no antigen, no action taken.

T cell TCR recognises ‘non-self’ antigen, specific t cells activated.

117
Q

Why do APCs only present to T cells?

A

Highly specific reaction between groove with foreign peptides on the surface and the T-cell receptor.

118
Q

What are the three classes of T cells?

A

Regulatory

Cytotoxic

Helper

119
Q

What does each of the three classes do?

A

Regulatory: inhibits function of other two classes and DC.

Cytotoxic: kills infected host by causing them to apoptise.

Helper: activate macrophages, DC, B cells and maintain cytootoxic activity by secreting cytokines.

120
Q

Why do cytotoxic T cells kill?

A

they recognise the antigens that were used to activate it on the target membrane, bind specifically to the cell.

The contact point forms an immunological synapse.

121
Q

What is the first strategy a cytotoxin T cell uses?

A

secretes perforins, which forms a channel in the target cell wall.

T cell then secretes proteases which activate caspases, the effector proteins in apoptosis.

122
Q

What is the second strategy used by Cytoxin t cells?

A

It will bind receptors to the target cell and activate caspases

123
Q

Where do b and t cell develop?

A

t cells in the thymus

b cells in the bone marrow

124
Q

how do B cells work?

A

soluble antigens in the blood or lymph

BCR recognises ‘self’ antigen, no action

BCR recognises no antigen, no action taken

BCR recognises ‘non-self’ antigen, activates specfiic B cells

125
Q

describe the antibodies basic structure

A

tetrameric, 4 polypeptide chains

2 identical Heavy chains and 2 identical Light chains.

Chains held together by covalent disulfide bonds at the hinge and between H x L.

126
Q

What are the different interactions that are experienced by antibodies?

A

One antibody tetramer can bind 2 identical antigens.

if antigen has 2 identical antigenic determinants, antibodies can cross-link the antigens, making cyclic complexes.

more identical antigenic determinants means 3D lattices can be formed.

127
Q

why is cross-linking in antigens so important?

A

cross-linking coupled with a flexible hinge region means soluble antigens and virus’ can be trapped in networks.

This makes it easier for phagocytes to engulf, amplifying the immune response.

128
Q

what is the collective name for antibodies?

A

immunoglobulins

129
Q

IgM, the most primitive immunoglobulin.

A

a pentamer of 5 antibodies, held by a J chain

first antibodies that a B cell makes.

over time, B cells switch to making other Ig molecules, new antibodiy forms retain the same specificity.

In pre-B cell, IgM are membrane-bound and form B cell receptors.

130
Q

How can IgM be selective?

A

immature B cell expresses IgM

movies to lymphoid tissue

mature B cells now express IgD too

Helper cells aid clonal expansion and differentiation.

Plasma cell now secretes IgM.

131
Q

what pathway is triggered by IgM

A

Classical

132
Q

How does IgM activate the complement?

A

phagocytic cells cannot recognise IgM.

IgM is considered an opsonin, anything assisting phagocytosis,

IgM efficient at activating the complement.

coating a target with IgM or complement is called opsonisation

133
Q

What are the functionns of IgG?

A

toxin neutralisation

opsonisation

passive immunity

134
Q

How is passive immunity gained through crossing the placenta?

A

Placental cells take up maternal IgG by pinocytosis.

Placental endosomes have receptors (FcRn) that bind to the tail region of IgG antibodies (Fc).

IgG molecules are transported across placental cells in vesicle carriers (transcytosis)

135
Q

How is passive immunity gained through maternal milk?

A

IgG secreted into mother’s milk.

FcRn receptors on neonatal gut cells recognise Fc of IgG antibodies.

IgG molcules are transported across the enterocytes by transcytosis.

Ig released into the neonatal circulation.

136
Q

What does IgA do?

A

protects mucosal surfaces

provides some passive immunity to newborns via milk.

137
Q

What does IgE do?

A

binds Fc receptors to mast cells, basophils and eosinophils.

it then acts as receptors for antigens.

138
Q

How does IgE trigger mast cell/basophil degranulation?

A

Mast cell captures IgE which binds to Fc

Multivalent antigen cross-links adjacent IgE molecules

Histamine release by exocytosis

histamine triggers blood vessel dilation and inflammation.

139
Q

How does IgE act as a receptor for eisonophils?

A

if larva is opsonised with complement or if eosinophils use IgE as receptor, eosinophils can recognise and kill it.

140
Q

what is class switching?

A

when mature B cells switch from IgM to other Ig classes, whilst maintaining the same specificity for the antigen.

This requires same Vh domain on a different heavy chain.

141
Q

what is somatic recombination of DNA?

A

chopping out unwanted DNA

142
Q

Summary of class switching:

A

antigen stimulates clonal expansion of B and T cells that have receptors which already recognise antigen.

Mature B cells produce IgM.

They can switch antibody heavy chain classes through somatic recombination, maintaining their variable domains and original specificity.

143
Q

What is the clonal selection theory?

A

antigen activates lymphocytes already committed to respond to it.

A lymphocyte committed to antigen displays cell surface receptors that specifically recognise the antigen.

When encountering which antigen they are committed to, lymphocytes will undergo clonal expansion and differentiation.

144
Q

What is clonal selection?

A

after infection, individual clones are selected by the antigen.

this results in pathogen-specific lymphocytes.

145
Q

where does diversity come from?

A

antigen specific receptors are encoded by unusual segmented genes.

They are assembled from a series of gene segments through somatic gene recombination.

Used for class switching, slight modification can lead to pre-existing diversity.

146
Q

How are antibodies so diverse?

A

3 antibody genes, 2 classes of light chains.

multiple gene segments encoding V domains that can be combined with C domains through somatic recombination.

This recombination selects a V gene and involves selecting pieces of diversity and joining DNA.

147
Q

what is affinity maturation?

A

over time, antibodies made by B cells improve in affinity and become more specific.

accumulation of point mutations in the V domains long after the coding sequences have been assembled from the segmented genes.

148
Q

What is the story of Affinity maturation?

A

Antigen stimulation causes activation and clonal expansion of B cells.

Some B cells proliferate and undergo somatic hypermutation, making antibodies with altered V domain specificity.

most will not be stimulated by the original antigen, will die.

Somme will have higher affinity and are copied.

149
Q

How is memory generated?

A

By the primary response.

after clonal expansion, T and B cells differentiate into effector cells.

Effector B cells secrete antibody, whereas T cells kill infected cells.

some antigen-stimulated cells multiply and differentiate into memory cells.

can become effectors by antigenic stimulation.

BS127: AIDs (3 decks)

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